MUSTARDE ROTATION FLAP AS ADEQUATE OPTION FOR HIGH-RISK BCC NEAR THE LOWER EYE LID: THE ADDITIONAL INTAKE OF...

Contamination of a heterogeneous class of drugs with nitrosamines of an also different type underlies or defines the occurrence of drug-induced skin cancer Nitrosogenesis or keratinocyte cancer Oncopharmacogenesis. Further identification of some of these carcinogens in drugs as both phototoxic and genotoxic in turn defines concepts such as Drug-Mediated Nitroso-Photo Carcinogenesis. Its first formal representative was and remains at present Nitrosomorpholine (Nmor). Unfortunately, further data on the propensity of individual nitrosamines and/or their derivatives to absorb photons and generate phototoxicity are lacking. The simultaneous intake of a heterogeneous class of drugs in the context of Nitrosocontamination, now officially announced by regulators, makes the initiation of cutaneous carcinogenesis a perfectly possible scenario. Continuous, permanent intake of several types of carcinogens/mutagens or nitrosamines in the context of potential/or real Nitrosocontamination is probably able to activate certain oncogenes such as RAS oncogenes and neutralize certain tumor suppressor genes such as p53. We report another case of a female patient who developed over the years 3 high-risk basal cell carcinomas in the facial area in a stepwise fashion in the context of potentially contaminated drug treatment with ACE inhibitor/Ramipril/Beta blocker/bisoprolol/, anticoagulant/ rivaroxaban/ and folic acid. The possible role of Nitroso contamination in polymedication in the context of drug related Nitroso-Photocarcinogenesis for the triggering of multiple basal cell carcinomas is commented. The performed Mustardé rotation flap for the tumour near the lower eyelid was with optimal final reconstructive result. Nitroso-Folic acid and Nitroso- Riviroxabanan are described for the first time in the medical literature as possible key elements that could have an activating effect on skin carcinogenesis on the background of the so-called metabolic reprogramming of the future tumour cell.